|Flow Cytometry (Flow)||3-5 µg/10^6 cells|
|Immunocytochemistry (ICC)||2 µg/ml|
|Immunofluorescence (IF)||2 µg/ml|
|Western Blot (WB)||1:100-1:1000|
|Immunohistochemistry (IHC)||See 2 publications below|
|Miscellaneous PubMed (MISC)||See 1 publications below|
|Western Blot (WB)||See 8 publications below|
|Tested Species reactivity||Human, Mouse, Rat|
|Published species reactivity||Rat , Mouse , Human|
|Host / Isotype||Rabbit / IgG|
|Immunogen||Synthetic peptide corresponding to residues L(20) M K G N K R E E Q G L G P E P A A P Q Q P T(42) C of Human alpha-Enac.|
|Purification||Antigen affinity chromatography|
|Storage buffer||PBS with 1mg/ml BSA|
|Contains||0.05% sodium azide|
|Storage conditions||-20° C, Avoid Freeze/Thaw Cycles|
PA1-920A detects alpha-epithelial sodium channel (alpha-ENaC) from human, mouse, and rat tissues and cells.
PA1-920A has been successfully used in Western blot procedures. By Western blot, this antibody specifically detects a ~97 kDa band representing glycosylated alpha-ENaC from NIH-3T3 cells, and a ~75 kDa band representing the unglycosylated alpha-ENaC protein from human brain samples.
The PA1-920A immunizing peptide is a synthetic peptide corresponding to residues 20-42 from human alpha-ENaC. This sequence is 82%, 73%, 64%, and 59% conserved in the rat and rabbit, mouse, guinea pig, and cow, respectively. PA1-920A immunizing peptide (Cat. # PEP-088) is available for use in neutralization and control experiments.
Epithelial sodium channels are amiloride-sensitive members of the degenerin/epithelial sodium channel (Deg/ENaC) superfamily of ion channels. Members of this superfamily of ion channels share organizational similarity in that they all possess two short intracellular amino and carboxyl termini, two short membrane spanning segments, and a large extracellular loop with a conserved cysteine-rich region. There are three homologous isoforms of the ENaC (alpha, beta, and gamma) protein. ENaC in the kidney, lung, and colon plays an essential role in trans-epithelial sodium and fluid balance. ENaC also mediates aldosterone-dependent sodium reabsorption in the distal nephron of the kidney, thus regulating blood pressure. ENaC is thought to be regulated, in part, through association with the cystic fibrosis transmembrane conductance regulator (CFTR) chloride ion channel. Gain-of-function mutations in beta- or gamma-ENaC can cause severe arterial hypertension (Liddel and quote;s syndrome) and loss-of-function mutations in alpha- or beta-ENaC causes pseudohypoaldosteronism (PHA-1).
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
Protein Aliases: alpha ENaC-2; Alpha-ENaC; alpha-epithelial sodium channel; Alpha-NaCH; amiloride-sensitive epithelial sodium channel; amiloride-sensitive epithelial sodium channel alpha subunit; Amiloride-sensitive sodium channel subunit alpha; amiloride-sensitive sodium channel subunit alpha 2; ENaC alpha; Epithelial Na(+) channel subunit alpha; epithelial sodium channel alpha subunit; nasal epithelial sodium channel alpha subunit; Nonvoltage-gated sodium channel 1 subunit alpha; SCNEA; sodium channel, non voltage gated 1 alpha subunit; sodium channel, non-voltage-gated 1 alpha subunit; sodium channel, nonvoltage-gated 1 alpha; sodium channel, nonvoltage-gated, type I, alpha; sodium channel, nonvoltage-gated, type I, alpha polypeptide
Gene Aliases: BESC2; ENaC; ENaCa; ENaCalpha; mENaC; Renac; SCNEA; SCNN1; SCNN1A
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